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Manganese levels increase in scrapie-infected sheep before..

flounder

Well-known member
Manganese levels increase in scrapie-infected sheep before clinical symptoms develop

Sheep infected with scrapie and cows infected with BSE have elevated levels of manganese in their blood before clinical symptoms appear, according to new research.

The findings, published in the Journal of Animal Science, also show that scrapie-resistant sheep produce elevated levels of the metal when “challenged” with the disease.

This suggests that elevated manganese levels in the blood and central nervous system are caused by the animal’s initial response to the disease.

The findings raise the possibility of using manganese levels in the blood as a potential diagnostic marker for prion infection. At present, only post-mortem examination of the brain tissue gives a certain diagnosis.

Scrapie, Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt-Jakob Disease (CJD) are neurodegenerative diseases that affect the brain and nervous system of sheep, cows and humans respectively.

They are transmitted by mis-formed prion proteins which cause tiny loss of brain cell in different regions of the brain, leading to impairment of brain function, including memory changes, personality changes and problems with movement that worsen over time.

“Definite diagnosis of prion disease is currently only possible post-mortem," said Professor David Brown from the University of Bath who led the study with colleagues from the universities of Hull and Edinburgh.

“These findings suggest that elevated blood manganese could be used as a robust diagnostic marker for prion infection, even before the onset of apparent clinical disease.

“In practice, however, it would be difficult implement a widespread screening programme, given that the mass spectrometry we use to measure levels is expensive and labour intensive.”

The research builds on the 2002 discovery that mice infected with scrapie have higher levels of manganese. This is the first time that tissue from farm animals infected with prion diseases have been studied in this way.

One of the most interesting findings from this study came from the analysis of blood samples from scrapie-resistant sheep.

When challenged with the disease, these sheep showed similar levels of manganese as non-resistant sheep challenged in the same way.

“Elevated levels of manganese in scrapie-resistant sheep imply that the change in blood manganese is a result of the scrapie challenge and not a consequence of scrapie pathology,” said Professor Brown, from the University of Bath’s Department of Biology & Biochemistry.

“Although these sheep are considered to be resistant to scrapie, they do show some indications that scrapie challenge results in similar metabolic changes as occur in non-resistant sheep.”

Another interesting finding was that although levels of manganese were elevated, there were differences in the blood levels of selenium and molybdenum in experimental and field cases of BSE in cows.

This suggests that the way a cow acquires the disease affects the metabolic processes involved.

“The origin of the increased manganese in the brains and blood of infected animals remains unknown,” said Professor Brown.

“The three possibilities are that there is decreased secretion of manganese from the body, release of manganese from other tissues or increased absorption of manganese from the environment.

“Currently there is insufficient evidence to favour any of these three theories.” -University of Bath

http://www.huliq.com/26192/manganese-levels-increase-in-scrapie-infected-sheep-before-clinical-symptoms-develop


Elevated manganese levels in blood and central nervous system occur before onset of clinical signs in scrapie and bovine spongiform encephalopathy
S. Hesketh*, J. Sassoon*, R. Knight, J. Hopkins and D. R. Brown*,1
* Department of Biology and Biochemistry, University of Bath, Bath, BA2 7AY, UK; and Department of Chemistry, University of Hull, Hull HU6 7RX, UK; and and Division of Veterinary Biomedical Sciences, University of Edinburgh, Edinburgh, EH9 1QH, UK

1 Corresponding author: [email protected]

Prion diseases, or transmissible spongiform encephalopathies, are neurodegenerative diseases that can only be accurately diagnosed by analysis of central nervous system tissue for the presence of an abnormal isoform of the prion protein known as PrPSc. Furthermore, these diseases have long incubation periods during which there are no clear symptoms but where the infectious agent could still be present in the tissues. Therefore, the development of diagnostic assays to detect a surrogate marker for the presence of prion disease is essential. Previous studies on mice experimentally infected with scrapie, an ovine spongiform encephalopathy, suggested that changes in the levels of Mn occur in the blood and brain before the onset of symptoms of the disease. To assess whether these findings have relevance to the animal diseases scrapie and bovine spongiform encephalopathy, tissues from bovine spongiform encephalopathy- and scrapie-infected cattle and sheep were analyzed for their metal content and compared with values for noninfected animals. In field cases and experimentally infected animals, elevated Mn was associated with prion infection. Although some central nervous system regions showed elevated Mn, other regions did not. The most consistent finding was an elevation of Mn in blood. This change was present in experimentally infected animals before the onset of symptoms. In scrapie-infected sheep, elevated Mn levels occurred regardless of the genotype of the sheep and were even detected in scrapie-resistant sheep in which no symptoms of disease were detected. These findings suggest that elevated blood Mn could be a potential diagnostic marker for prion infection even in the absence of apparent clinical disease.

http://jas.fass.org/


TSS
 

Mike

Well-known member
Are the manganese levels elevated because of the disease or is the disease because of the elevated manganese levels?

Kathy is going to wear you out on this this kiddo. :lol:
 

rkaiser

Well-known member
“The origin of the increased manganese in the brains and blood of infected animals remains unknown,” said Professor Brown.

“The three possibilities are that there is decreased secretion of manganese from the body, release of manganese from other tissues or increased absorption of manganese from the environment.

“Currently there is insufficient evidence to favour any of these three theories.” -University of Bath

Sounds like an unknown that needs a bit of knowing to me.

Which of the three do you think it is Terry?
 

flounder

Well-known member
hello mike, rkaiser et al,

mike wrote ;

> Are the manganese levels elevated because of the disease or is the disease because of the elevated levels?

> Kathy is going to wear you out on this this kiddo.


yep, i figured she might take the football and run. but when science shows that metals, op's, nuclear proliferation, or anything else _causes_ TSEs, beside what we know already, from the oral route, to the proven environmental factors, friendly fire, i will go with it. until then, i will stand by what i have stated all along, 'amplification and transmission'. i have not wavered from that. i have even stated in that past that metals may play a role in one's _susceptibility_, but we must stop what we already know, amplification and transmission. we must not waiver from that. ...terry



rkaiser wrote ;

> Sounds like an unknown that needs a bit of knowing to me.

> Which of the three do you think it is Terry?


confusious asks below, but you gotta read through first rkaiser :wink:


Subject: FATEPriDE Environmental Factors that Affect the Development of Prion Diseases
Date: February 18, 2006 at 9:24 am PST

FATEPriDE


Environmental Factors that Affect the Development of Prion Diseases.

Project funded by the European Commission under the Quality of Life Programme.


Contract No: QLK4-CT-2002-02723

Project No: QLRT-2001-02723

Start Date

1st January 2003

Duration

36 months plus 6 month extension

Partners

1. The University of Bristol, UK (Co-ordinator)
2. National Environment Research Council-The British Geological Society, UK
3. University of Bath, UK
4. Free University of Berlin, Germany
5. University of Iceland, Iceland
6. Universita degli studi di Perugia, Italy
7. Universite Joseph Fourier Grenoble, France
8. Alpine Institute of Environmental Dynamics, France

Introduction

The work proposed here brings together top EU geo and biochemists focusing on determining the environmental factors that affect the development of prion diseases such as scrapie, bovine spongiform enchpalitis (BSE), chronic wasting disease (CWD) and Creutzfeld-Jacobs disease (CJD). First the geographical distribution of manganese and copper in soils will be investigated as risk factors. This will be undertaken due to the fact that prion diseases often are found in clusters. It now has been established that the normal metal for prion protein is copper but if that metal is replaced with manganese, the structure of the prion protein is altered. The role of organophosphate pesticides will also be investigated because it has been suggested that copper is complexed with organophosphate, preventing copper absorption.

Objectives

There is clear evidence that the occurrence of prion diseases often has a non-random distribution, suggesting a link to some environmental factors. The work proposed here will investigate risk factors, including the role of trace elements and organophosphates. Analysis of regional variation in local manganese/copper levels will be determined and compared to the incidence of the diseases. The ability of manganese and/or organophosphates in influencing conversion of the prion protein to an abnormal and/or infectious protein will be determined. In combination with geographical occurrence and geo-chemical considerations this program will identify whether these environmental considerations should be acted upon to bring about effective prevention or at least risk minimalisation of prion diseases in the EU and further afield.

Description of the Work

Recently it has been suggested that disbalance in dietary trace-elements and/or exposure to organophosphates might either cause or be a risk factor for prion disease development. In particular, high incidence of scrapie (e.g. in Iceland), chronic wasting disease, and in Slovakia and Italy CJD are associated with regions where soil and foliage are reported to be low in copper and high in manganese. This proposal will address whether exposure to a diet that has a high manganese/copper ratio can influence prion disease will also be addressed. In particular, we shall investigate this theory at the level of protein, cells, animals as well as geographical and geo-chemical associations with prion diseases. Animal models of prion disease and sheep from farms in regions of high scrapie will be investigated for a possible influence of level of manganese and copper on incidence or onset of these diseases. Bio-chemical and biophysical techniques will be used to investigate interaction of the prion protein with copper and manganese to determine the mechanism by which Mn substitution for Cu influences conversion to the abnormal isoform of the protein and whether such conversion results in protein that is infectious in mouse bioassay for infectivity. Additionally, a cell culture model will be used to generate abnormal prion protein by exposure to manganese. Cell culture model of infection will be used to assay whether prion disease alters manganese metabolism and transport of manganese into cells. The level of expression of the prion protein is in itself a risk factor for prion disease as it shortens the incubation time for the disease. This research will result in understanding of the role of disbalance in the trace elements Cu and Mn on the onset and mechanisms behind the occurrence of prion diseases and will for the first time define whether there are environmental risk factors for prion diseases.

Milestones and Expected Results

The study proposed here will produce a geo-chemical map of Europe for manganese and copper. These maps will be used to target field areas where prion diseases have occurred as clusters. The bio-chemical studies will establish whether the replacement of manganese for copper in prion protein is a risk factor for the disease _development_. Organophosphate will also be investigated as a risk factor. The study aims at minimising the risk of prion diseases for humans and animals in the EU.



http://www.arp-manchester.org.uk/FatePride.htm


SINCE THEN ;


Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE
Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were
carried out throughout the project. No relationship between this
compound and the potential to cause a TSE were identified. In
studies with oral dosing of rats, it was shown that PrP expression
levels increased in the brain but there was no association between
this and formation of proteinase K (PK) resistant PrP.


snip...


12. A model of seed protein aggregation and fibril formation was
established using PrP charged with Mn2+. PrP-Mn2+ was found to
form small circular aggregates able to catalyse further protein
aggregation and fibrilisation of PrP. This model unlike other
published models (for example those of Baskakov et al.1) does not
require the presence of denaturants and is not an autocatalytic
process (i.e. the substrate of the reaction did not aggregate). The
results suggest that Mn2+ may play a role in the formation of prion
seeds

__although further studies showed that this material was not
infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of
TSEs to environmental factors:
• __Potentially no role for organophosphates in TSEs.__
• Increased Mn in the diet results in higher PrP levels in the
brain.
• No conclusion is yet possible in terms of the relationship
between environmental trace element concentrations and the
geographical occurrence of TSEs (classical scrapie or BSE).
• Some confirmation was provided that in some specific farms
occurrence of classical scrapie correlates with high Mn levels.


http://www.seac.gov.uk/papers/97-4.pdf



a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines – addressed in the enquiries – provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf



transmission studies do not lie, amplification and transmission!


1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf



and for Gods sake, if someone is smearing this [email protected] all over there kids
heads for lice and did not come up with a TSE, i would say this is good case study;


UK FARMER WITH BSE


1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....


However, i have never dusputed the remote possibility that ;


Phosmet induces up-regulation of surface levels of the cellular prion protein.
Neuroreport. 9(7):1391-1395, May 11, 1998.
Gordon, Irit 1; Abdulla, Elizabeth M. 1; Campbell, Iain C. 1; Whatley, Stephen A. 1,2
Abstract:
CHRONIC (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the _susceptibility to the prion agent by altering the levels of accessible PrP_.

(C) Lippincott-Raven Publishers.


http://www.neuroreport.com/

http://www.ranchers.net/forum/about15704-0-asc-60.html


o.k. rkaiser, here ya go ;


confusious asks, could some of the ingredients releasing of manganese from other tissues or, increased absorption of manganese from
the environment in these feeds be causing the _susceptibility_ of the TSE agent spread, via animal protein transmission ???



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http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&P=19137


https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument


WHEN/IF science ever shows that any op's, metals, nuclear proliferation, or anything else _causes_ TSEs, beside what we know already
via oral route, friendly fire, to the proven environmental factors, i will be the first to admit i was wrong. that has not happened to date.


o.k. girlfriend, lay it on me :wink:


terry
 

rkaiser

Well-known member
Nothing to lay on girlfreind -

I will welcome the day when you "admit you was wrong".

Quote:
“The origin of the increased manganese in the brains and blood of infected animals remains unknown,” said Professor Brown.

“The three possibilities are that there is decreased secretion of manganese from the body, release of manganese from other tissues or increased absorption of manganese from the environment.

“Currently there is insufficient evidence to favour any of these three theories.” -University of Bath

I will ask again Terry - which of the three do you think is causing elevated manganese?
 

flounder

Well-known member
rkaiser said:
Nothing to lay on girlfreind -

I will welcome the day when you "admit you was wrong".

Quote:


please explain what i am wrong about rkaiser.

are you saying that the amplification and transmission of tainted feed did not cause the drastic increase in UK BSE, and then when ban was implemented, the drastic decrease ???


please explain you position rkaiser. we hear a lot of whinning, but nothing to back it up ???


your saying the transmission studies mean nothing, it's all metals, and feed has nothing to do with it ???

show me the data............

tss
 

rkaiser

Well-known member
You're the one who said you would admit when you are wrong about metals Terry. I was just wishing the day would come sooner rather than later.

As far as producing data - you go ahead Terry - post another few million words about the tainted feed theory. I have said before and will say again that if it was tainted - it was tainted with metals and not your magical misfolded prion which somehow defies the law of the universe and makes it's way from the stomach of a cow to it's brain. :roll:

No whinning here Terry dear - that is all for you. How many times do we have to say that we feel for your loss?

Now quit wasting your time and push for BSE testing or something positive rather than trying to blame cows for hell on earth.
 

rkaiser

Well-known member
man! man! man!

not cows...............

terry

You got er Terry - Man and his influence on the environment. All of the TSE clusters that Mark Purdey investigated were in areas where "Man" had screwed with the environment.

In fact - forget Mark for a moment (rest his soul) All TSE situations period are caused by man and his relentless desire to screw with the environment.
 

flounder

Well-known member
ITEM 6 FATEPRIDE (SEAC 97/4)
35. The Chair explained that FATEPriDE is a multi-centre European
Union funded project that examined the possible influence of
environmental trace elements on the occurrence of TSEs.
36. Professor David Brown (University of Bath) explained that the
project had principally studied potential interactions between prion
disease and copper and manganese, although interactions with
other environmental factors such as organophosphates had also
been assessed. No link, other than with manganese, between
many environmental factors studied, including organophosphates,
and TSEs was found. The key experiments and findings had been
summarised in SEAC paper 97/4. The main conclusions were that
manganese binds to PrP with similar affinity to known manganese
binding proteins, induces conformational change in PrP, catalyses
PrP aggregation, induces protease resistance in PrP, increases
PrP expression levels and increases cellular susceptibility to prion
infection. Manganese had also been found at high levels on farms
with a high classical scrapie incidence and manganese was found
to increase the stability of PrP in soil. Although it had been the
intention to create maps of bioavailable manganese and compare
those to similar maps of TSE hotspots, this had not been possible
as no data of sufficient precision relating the location of BSE or
scrapie cases was made available. Further studies were required
to investigate the interactions of manganese and prions.


37. Members noted that the study suggested an association between
high levels of bioavailable manganese, low levels of bioavailable
copper and classical scrapie in field studies. However, it was likely
that other factors such as soil pH and organic matter may also be
involved. It was acknowledged that it was very difficult in
environmental studies to exclude potential confounding factors.
The experimental and field data suggested that manganese may
influence the susceptibility to TSEs.

However, there was no
evidence that environmental factors, including manganese, cause
disease.


38. Members noted that data on BSE should allow spatial mapping of
cases, however sheep movements were so complex that it is not
possible to create similar maps for classical or atypical scrapie.
39. Members suggested that further research could investigate the
differential stability of a range of TSE agents bound with
manganese in soil, although other modifying factors in soil such as
12
© SEAC 2006
soil content and pH are likely. In addition, further animal studies
could examine the effect of manganese on a range of TSE agents.


http://www.seac.gov.uk/papers/draft98-1.pdf
 

Kathy

Well-known member
Terry's bored today... you got nothing better to do that post here I see.

We are busy haying and I thought I'd check in to see if anything important was added.

But it is just Terry rehashing the old stuff.

A copper loaded prion proteion is the healthy version of the prion protein. When copper does not bind to it and another metal, such as manganese (or any other PARAMAGNETIC metal) then this allows for the metal nucleating centers to nucleate the contaminated proteins. Copper is not paramagnetic.
 
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